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Background Systemic sclerosis (SSc) causes progressive fibrosis of multiple organs with the low efficacy of immunosuppressive therapies. Our previous study indicated the SSc pathological pathways are closely correlated with Ca2+ signals, and blockage of the intracellular Ca2+ elevation facilitates inhibition of SSc pathogenesis. Objective Transforming growth factor β (TGF-β)-modulated SMAD signaling is crucial in regulating SSc pathogenesis. Whether Ca2+ signals are involved in TGF-β1/SMAD signaling-induced fibrotic process has been further investigated. Methods We utilized TGF-β1-induced myofibroblasts as a model to detect how Ca2+ signals affected SSc pathogenesis, and investigated the combination of treatment with store-operated Ca2+ entry (SOCE) associated inhibitors, 2-aminoethyl diphenylborinate (2-APB) and SKF96365 to restrain the increased Ca2+ signaling in myofibroblasts. In addition, the SSc bleomycin mouse model was used to detect the effect of 2-APB on SSc pathogenesis in vivo. Results Our findings revealed increased levels of TGF-β1 production in SSc was associated with intracellular Ca2+ activity, and inhibition of intracellular Ca2+ regulation by 2-APB resulted in the dedifferentiation of TGF-β1-induced myofibroblasts. This was due to the fact that 2-APB restrained the expression fibrotic markers, α-SMA, fibronectin and vimentin through inhibiting TGF-β1/SMAD3 signaling. Thus, subcutaneous injection of 2-APB improved bleomycin-induced skin and pulmonary fibrosis. Conclusion 2-APB is a potential candidate for treating fibrosis, by disrupting intracellular Ca2+ regulation in SSc to induce the dedifferentiation of myofibroblasts and meliorates fibrosis pathogenesis via inhibiting TGF-β1/SMAD3 signaling.

Despite expanding knowledge regarding the role of astroglia in regulating neuronal function, little is known about regional or functional subgroups of brain astroglia and how they may interact with neurons. We use an astroglia-specific promoter fragment in transgenic mice to identify an anatomically defined subset of adult gray matter astroglia. Using transcriptomic and histological analyses, we generate a combinatorial profile for the in vivo identification and characterization of this astroglia subpopulation. These astroglia are enriched in mouse cortical layer V; express distinct molecular markers, including Norrin and leucine-rich repeat-containing G-protein-coupled receptor 6 (LGR6), with corresponding layer-specific neuronal ligands; are found in the human cortex; and modulate neuronal activity. Astrocytic Norrin appears to regulate dendrites and spines; its loss, as occurring in Norrie disease, contributes to cortical dendritic spine loss. These studies provide evidence that human and rodent astroglia subtypes are regionally and functionally distinct, can regulate local neuronal dendrite and synaptic spine development, and contribute to disease.

Systemic sclerosis (SSc) causes progressive fibrosis of multiple organs with the low efficacy of immunosuppressive therapies. Our previous study indicated the SSc pathological pathways are closely correlated with CaTransforming growth factor β (TGF-β)-modulated SMAD signaling is crucial in regulating SSc pathogenesis. Whether CaWe utilized TGF-β1-induced myofibroblasts as a model to detect how CaOur findings revealed increased levels of TGF-β1 production in SSc was associated with intracellular Ca2-APB is a potential candidate for treating fibrosis, by disrupting intracellular Ca

BACKGROUND Drug reaction with eosinophilia and systemic symptoms (DRESS) is a condition caused by a drug-induced immune response. Previous reports have found that CXCL10, also known as interferon-γ-induced protein (IP)-10, may participate in the pathogenesis of cutaneous adverse drug reactions. However, the exact role of IP-10 in DRESS and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) has remained unknown. OBJECTIVES This comparative prospective cohort study aimed to ascertain the roles of the IP-10/CXCR3 axis in DRESS and SJS/TEN. METHODS Plasma IP-10 levels were analysed, and univariate analyses were conducted to assess the relationship between IP-10, human herpesvirus (HHV)-6 reactivation and the development of long-term sequelae. We also performed immunohistochemical staining using skin specimens and flow cytometry to determine the expression of CXCR3 in peripheral blood mononuclear cells (PBMCs). RESULTS Significantly higher plasma IP-10 levels were observed in patients with DRESS with long-term sequelae (effect size 0·81) and also in those with HHV-6 reactivation (effect size 0·83). By immunohistochemistry, more abundant IP-10+ and CXCR3+ cells were demonstrated in the skin lesions of patients with DRESS with HHV-6 reactivation. The percentages of CLA+ CXCR3+ CD4+ cells and CLA+ CXCR3+ CD8+ cells were also higher in the PBMCs of HHV-6-reactivated patients with DRESS than in those of patients with SJS/TEN. CONCLUSIONS Higher plasma IP-10 levels are associated with the development of long-term sequelae in DRESS. Higher IP-10/CXCR3 expression in skin and more abundant CLA+ CXCR3+ CD4+ cells and CLA+ CXCR3+ CD8+ cells were observed in patients with DRESS with HHV-6 reactivation. The IP-10/CXCR3 axis is associated with HHV-6 reactivation and development of long-term sequelae in DRESS. What is already known about this topic? Elevated levels of interferon-γ-induced protein-10 (IP-10) have been observed in patients with drug reaction with eosinophilia and systemic symptoms (DRESS) and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN). Patients with DRESS tend to develop long-term autoimmune sequelae, including type 1 diabetes and autoimmune thyroiditis. IP-10 has been associated with these autoimmune diseases in previous studies. What does this study add? The patients with DRESS with HHV-6 reactivation exhibited higher levels of IP-10 in the plasma and skin than the patients with DRESS without HHV-6 reactivation and the patients with SJS/TEN. Patients with DRESS with higher plasma IP-10 levels tended to develop sequelae during long-term follow-up. What is the translational message? IP-10 is a useful biomarker to predict the development of long-term sequelae in patients with DRESS. Linked Comment: Belloon and Kardaun. Br J Dermatol 2020; 183:804-805.

Background/Objective There is a rising awareness of drug reaction with eosinophilia and systemic symptoms (DRESS) due to its possible morbidity and mortality. Early diagnosis of DRESS is crucial for administering timely treatment; however, prompt diagnosis based on its early presentation can be quite problematic due to its clinical resemblance to common maculopapular eruptions (MPE). Methods A retrospective cohort study of patient data from September 2010 to June 2016 was conducted to compare the clinical presentations of DRESS and MPE validated by the RegiSCAR scoring system. The demographic data, clinical presentations, and histopathological patterns were reviewed. Results Fifty-eight patients with DRESS and 29 patients with MPE were included. The mean age at diagnosis of DRESS was 47 years (range: 2–82 years), and female patients predominated by a ratio of 2.2:1. The three most common culprit medications for DRESS were allopurinol, sulfasalazine, and trimethoprim/sulfamethoxazole. The most significant differences between the DRESS and MPE groups were the presence of fever, peripheral blood eosinophilia and atypical lymphocytosis, characteristic skin lesions, abnormal liver functions, and prolonged resolution of skin lesions for more than 15 days in the DRESS patients. The most common histologic features in the DRESS patients were coexistent eczematous, interface dermatitis, and vascular damage patterns, or interface dermatitis alone. The concurrence of fever, peripheral blood eosinophilia, and abnormal liver function within three days of visiting a medical facility were more common in cases of DRESS than of MPE (24.1% vs. 0%, P = 0.004). Conclusion Although DRESS and MPE look similar, especially in the early stage of DRESS, the concurrence of fever, peripheral blood eosinophilia, and abnormal liver functions within three days of visiting a medical facility might aid in the early diagnosis of DRESS.

A series of donor-acceptor-donor triazine-based molecules with thermally activated delayed fluorescence (TADF) properties were synthesized to obtain highly efficient blue-emitting OLEDs with non-doped emitting layers (EMLs). The targeted molecules use a triazine core as the electron acceptor, and a benzene ring as the conjugated linker with different electron donors to alternate the energy level of the HOMO to further tune the emission color. The introduction of long alkyl chains on the triazine core inhibits the unwanted intermolecular D-D/A-A-type π-π interactions, resulting in the intermolecular D-A charge transfer. The weak aggregation-caused quenching (ACQ) effect caused by the suppressed intermolecular D-D/A-A-type π-π interaction further enhances the emission. The crowded molecular structure allows the electron donor and acceptor to be nearly orthogonal, thereby reducing the energy gap between triplet and singlet excited states (ΔEST ). As a result, blue-emitting devices with TH-2DMAC and TH-2DPAC non-doped EMLs showed satisfactory efficiencies of 12.8 % and 15.8 %, respectively, which is one of the highest external quantum efficiency (EQEs) reported for blue TADF emitters (λpeak

This paper presents the design of three millimeter-wave and terahertz signal sources that demonstrates the feasibility of high performance signal source implemented in CMOS. A triple-push oscillator consisted of two antiparallel LC ring oscillators is presented with a low phase noise of −88 dBc/Hz at 1-MHz offset and a peak output power of −6 dBm at 210 GHz in a 90-nm CMOS process. An injection locked quadruple-push oscillator is then presented with a simulated output power of −16.3 dBm at 336 GHz and phase noise of −88 dBc/Hz at fundamental frequency in a 90-nm CMOS process. Lastly, a 330-GHz subharmonic injection locked frequency synthesizer is proposed. The core oscillator is based on the triple-push architecture. The frequency synthesizer achieves a simulated locking range of 5 GHz at 330 GHz with an output power of −8.6 dBm in a 40-nm CMOS process.

Aging, cancer, and longevity have been linked to intracellular Ca2+ signaling and nociceptive transient receptor potential (TRP) channels. We found that TRP canonical 7 (TRPC7) is a nociceptive mechanoreceptor and that TRPC7 channels specifically mediate the initiation of ultraviolet B (UVB)‐induced skin aging and tumor development due to p53 gene family mutations. Within 30 min after UVB irradiation, TRPC7 mediated UVB‐induced Ca2+ influx and the subsequent production of reactive oxygen species in skin cells. Notably, this function was unique to TRPC7 and was not observed for other TRP channels. In TRPC7 knockout mice, we did not observe the significant UVB‐associated pathology seen in wild‐type mice, including epidermal thickening, abnormal keratinocyte differentiation, and DNA damage response activation. TRPC7 knockout mice also had significantly fewer UVB‐induced cancerous tumors than did wild‐type mice, and UVB‐induced p53 gene family mutations were prevented in TRPC7 knockout mice. These results indicate that TRPC7 activity is pivotal in the initiation of UVB‐induced skin aging and tumorigenesis and that the reduction in TRPC7 activity suppresses the UVB‐induced aging process and tumor development. Our findings support that TRPC7 is a potential tumor initiator gene and that it causes cell aging and genomic instability, followed by a change in the activity of proto‐oncogenes and tumor suppressor genes to promote tumorigenesis., Schematic representation of the role of TRPC7 as a potential tumor initiator gene in ultraviolet B (UVB)‐induced aging and cancer progression. UVB‐activated TRPC7 initiates skin aging via intracellular Ca2+ elevation, resulting in oxidative stress, DNA damage response activation, abnormal differentiation, and senescence inflammation response activation; this pathology is repaired with the activation of p53 to maintain tissue homeostasis. When homeostasis is no longer maintained and the aging process is activated, carcinogens promote cancer progression. TRPC7 initiates tumorigenesis by causing genomic instability, thereby changing the activity of proto‐oncogenes and tumor suppressor genes.

The adsorption and dehydrogenation of water on Fe(111), W@Fe(111), and W2@Fe(111) surfaces have been studied via employing the first-principles calculations method based on the density functional theory. The three adsorption sites of the aforesaid surfaces, such as top (T), 3-fold-shallow (S), and 3-fold-deep (D), were considered. The most favorable structure of all OHx (x = 0–2) species on the surfaces of Fe(111), W@Fe(111), and W2@Fe(111) have been thoroughly predicted and discussed. Our calculated results revealed that the adsorbed configurations of FeH2O(T-η1-O)-b, W@FeH2O(T-η1-O)-a, and W2@FeH2O(T-η1-O)-a possess energetically the most stable structure with their corresponding adsorption energies of −8.08, −13.37, and −18.61 kcal/mol, respectively. In addition, the calculated activation energies for the first dehydrogenation processes (HO-H bond scission) of H2O on Fe(111), W@Fe(111), and W2@Fe(111) surfaces are 24.40, 12.62, and 9.97 kcal/mol, respectively. For second dehydrogenation processes (O–H ...

Background: Plasmacytoid dendritic cells (pDCs) are implicated in the reactivation of human herpesvirus 6 (HHV-6) in drug reaction with eosinophilia and systemic symptoms (DRESS). Objectives: We aimed at identifying the alterations of circulating pDCs, basophils, and myeloid dendritic cells (mDCs) during the active stage of drug eruptions and the relationship between pDC alteration and HHV-6 reactivation in DRESS patients. Methods: Nine DRESS patients and twelve patients of other drug eruptions (ODE, including five cases of maculopapular eruptions (MPEs), five cases of Stevens–Johnson syndrome, and two cases of fixed drug eruption) were prospectively recruited. Blood samples were collected weekly for 2 consecutive weeks for flow cytometry of pDC, basophil, mDC, and detection of HHV-6 reactivation by serum anti-HHV-6 immunoglobulin G, or whole blood HHV-6 viral DNA by quantitative polymerase chain reaction. Results: The HHV-6 reactivation was exclusively seen in DRESS, and the pDC levels decreased in DRESS compared with ODE (P = 0.002) and (MPE, P = 0.021), with the timing of such decrease preceding HHV-6 reactivation. Conclusion: The decrease of pDC levels is significantly more common in DRESS patients and occurs before HHV-6 reactivation. The chronological sequence implies that the decrease of pDC may be crucial in the pathogenesis of viral reactivation.

Astroglia are the most abundant glia cell in the central nervous system, playing essential roles in maintaining homeostasis. Key functions of astroglia include, but are not limited to, neurotransmitter recycling, ion buffering, immune modulation, neurotrophin secretion, neuronal synaptogenesis and elimination, and blood–brain barrier maintenance. In neurological diseases, it is well appreciated that astroglia play crucial roles in the disease pathogenesis. In amyotrophic lateral sclerosis (ALS), a motor neuron degenerative disease, astroglia in the spinal cord and cortex downregulate essential transporters, among other proteins, that exacerbate disease progression. Spinal cord astroglia undergo dramatic transcriptome dysregulation. However, in the cortex, it has not been well studied what effects glia, especially astroglia, have on upper motor neurons in the pathology of ALS. To begin to shed light on the involvement and dysregulation that astroglia undergo in ALS, we isolated pure grey-matter cortical astroglia and subjected them to microarray analysis. We uncovered a vast number of genes that show dysregulation at end-stage in the ALS mouse model, G93A SOD1. Many of these genes play essential roles in ion homeostasis and the Wnt-signaling pathway. Several of these dysregulated genes are common in ALS spinal cord astroglia, while many of them are unique. This database serves as an approach for understanding the significance of dysfunctional genes and pathways in cortical astroglia in the context of motor neuron disease, as well as determining regional astroglia heterogeneity, and providing insight into ALS pathogenesis.

The dysfunction of voltage-gated ion channels contributes to the pathology of ischemic stroke. In this study, we developed rat models of transient ischemic attack (TIA) and reversible ischemic neurological deficit (RIND) that was induced via the injection of artificial embolic particles during full consciousness, that allow us to monitor the neurologic deficit and positron emission tomography (PET) scans in real-time. We then evaluated the infarction volume of brain tissue was confirmed by 2,3,5-triphenyl tetrazolium chloride (TTC) staining, and gene expressions were evaluated by quantitative real-time PCR (qPCR). We found that rats with TIA or RIND exhibited neurological deficits as determined by negative TTC and PET findings. However, the expression of voltage-gated sodium channels in the hippocampus was significantly up-regulated in the qPCR array study. Furthermore, an altered expression of sodium channel β-subunits and potassium channels, were observed in RIND compared to TIA groups. In conclusion, to our knowledge, this is the first report of the successful evaluation of voltage-gated ion channel gene expression in TIA and RIND animal models. This model will aid future studies in investigating pathophysiological mechanisms, and in developing new therapeutic compounds for the treatment of TIA and RIND.

Lattice structures, including reflection lattice planes and lattice constant, of liquid-crystal blue phase I (BPI) are studied via the measurements on reflection spectrum and Kossel diagram as concentration of a chiral dopant is changed. Peaks of the reflection wavelength in BPI are mainly dominated by the lattice plane and the lattice constant, which are affected by the chiral concentration. In the chiral nematic state, as decreasing the chiral concentration the reflection peak will shift to a longer wavelength because the helical pitch linearly depends on the chiral concentration and becomes longer. However, this dependence of the chiral concentration and reflection wavelength is broken in the BPI. The reflection peak of BPI moves to a short wavelength when the chiral concentration is less due to the contraction of the lattice constant as well as helical pitch. Moreover, when the concentration of the chiral dopant increases over a certain value, a discontinuous shift in reflection peak occurs due to the...

The subventricular zone (SVZ) is a proliferative region that provides neurons to olfactory bulb throughout life. The new neurons undergo cell migration from SVZ and travel until they reach their final destination. We previously showed in the early postnatal mouse a ventral migratory subpopulation from SVZ targets the Islands of Calleja (ICC) in the basal forebrain. However, unlike the well-characterized rostral migratory stream, little is known about the guidance mechanisms operating in the ventrally directed migratory pathway. In this study, we examined the role of neurotransmitter γ-aminobutyric acid (GABA) in SVZ-derived progenitor ventral migration and the involvement of this neurotransmitter in the cytoarchitectual organization of dispersed cells into the tight clusters of the ICC. Our results show that the ventral SVZ cell migration rate was enhanced by GABA acting through a GABAA receptor and that GABA acts as a directional guidance cue for ventral migrating cells. Furthermore, disruption of GABA signaling inhibited the formation of Island clusters in vitro. Taken together, these data suggest that GABA is an important guidance and organizational cue for the Island of Calleja.

In this study, we explore a relation between reflection colors and a chiral concentration. Basing on our observation, the reflection colors in BPI are dominated by lattice surface of the platelets and the lattice constant of a unit cell, but they do not depend linearly on the chiral concentration. The reflection peak moves to a short wavelength as increasing the chiral concentration because of contracting the lattice constant. However, when the lattice plane is changed, the reflection is dominated by the lattice plane, and it may move to a longer wavelength.

A 10-bit 200 MS/s pipeline ADC using the capacitor-sharing concept is presented. A charge-neutralization technique is proposed between the 1st and 2nd MDACs to mitigate the memory effect. To further enhance power efficiency, a reference precharge technique is proposed between the 2nd and 3rd MDACs. The prototype ADC in 90-nm low-power CMOS process exhibits an INL of + 1.59/-1.91 LSB and a DNL of +0.70/-0.75 LSB. Its ENOB is 8.53 bits at input frequency of 2 MHz and 8.05 bits at Nyquist input frequency with the conversion rate of 200 MS/s. It consumes 45.4 mW at 1.2 V supply and occupies an active chip area of 0.53 mm2.

A home-based motion-sensing tele-rehabilitation system that incorporated motion-sensing technology and cloud technology was developed for improving the rehabilitation mode of patients with frozen shoulder. The system will enable the patients to carry out motion-sensing rehabilitation at home and its rehabilitation results can be calculated and analyzed instantly in terms of motion effect index with cloud computing technology. The system will also enable medical professionals to find out patients rehabilitation status via a cloud system and issue personalized prescriptions of home-based rehabilitation system for individual patients.

The Islands of Calleja are aggregations of granule cells located in the basal forebrain of most vertebrate species. These cellular aggregations are typically classified as consisting of a single island, the insula magna located adjacent to the nucleus accumbens, and numerous small islands scattered among the dorsal aspect of the olfactory tubercle. While these structures have been widely described in adult, comparatively little is known about their development. Islands are first identifiable at P2–P4 with formation of the Insula Magna and several small aggregations in the caudolateral aspect of the basal forebrain. The Insula Magna fully forms at approximately P4, with continued formation of the small islands through P10 in a caudal to rostral gradient. Historically, there has been controversy as to whether neurons in the islands are GABAergic, due to limitations in resolving immunolabeling for GABA in the densely packed islands. We investigated the neurochemical identity of island cells by exploiting transgenic reporter mice expressing green fluorescent protein under the control of the GAD65 promoter. This demonstrated that the majority of neurons in the Islands of Calleja are GABAergic, primarily utilizing GAD65. Interestingly, several calcium binding protein expressing interneuron classes are present in the postnatal islands, but disappear with maturation. These findings show that the SVZ derived progenitors that migrate to the Islands of Calleja form different lineages to those destined for the olfactory bulbs, despite generation of both populations at the same age/location in the SVZ.

Ultrasonic harmonic imaging provides superior image quality than linear imaging and has become an important diagnostic tool in many clinical applications. Nevertheless, the contrast-to-tissue ratio (CTR) in harmonic imaging is generally limited by tissue background signal comprising both the leakage harmonic signal and the tissue harmonic signal. Harmonic leakage generally occurs when a wideband transmit pulse is used for better axial resolution. In addition, generation of tissue harmonic signal during acoustic propagation also decreases the CTR. In this paper, suppression of tissue background signal in harmonic imaging is studied by selecting an optimal phase of the transmit signal to achieve destructive cancellation between the tissue harmonic signal and the leakage harmonic signal. With the optimal suppression phase, our results indicate that the tissue signal can be significantly reduced at second harmonic band, whereas the harmonic amplitude from contrast agents shows negligible change with the selection of transmit phase. Consequently, about 5-dB CTR improvement can be achieved from effective reduction of tissue background amplitude in optimal transmit phasing.

New cells are continuously added to the rodent olfactory bulb (OB), throughout development and in adults. These cells migrate tangentially from the subventricular zone along the rostral migratory stream to the OB, where they migrate radically from the center to periphery of the OB. Although different modalities of radial migration have been described in other brain regions, the mechanisms governing radial migration in the OB are still mostly unknown. Here, we identify a new modality of migration in which neuronal precursors migrate along blood vessels toward their destination. Our results show that half of the radially migrating cells associate with the vasculature in the granule cell layer of the OB, andin vivotime-lapse imaging demonstrates that they use blood vessels as a scaffold for their migration through an interaction with the extracellular matrix and perivascular astrocyte end feet. The present data provide evidence that a new modality of migration, vasophilic migration, is occurring in the adult brain and reveals a novel role of brain vasculature.

The subventricular zone (SVZ) of the lateral ventricle develops from residual progenitors of the embryonic lateral ganglionic eminence (LGE) and maintains neurogenic activity throughout life. Precursors from LGE/SVZ migrate to the olfactory bulb (OB) where they differentiate into local interneurons, principally in the granule layer and glomerular layer (GL). Byin situdye labeling, we show that neonatal and adult SVZ progenitors differentially contribute to neurochemically distinct types of periglomerular interneurons in the GL. Namely, calbindin-positive periglomerular cells are preferentially generated during early life, whereas calretinin- and tyrosine hydroxylase-expressing neurons are mainly produced at later ages. Furthermore, homochronic/heterochronic transplantation demonstrates that progenitor cells isolated from the LGE or SVZ at different stages (embryonic day 15 and postnatal days 2 and 30) engraft into the SVZ of neonatal or adult mice, migrate to the OB, and differentiate into local interneurons, including granule and periglomerular cells as well as other types of interneurons. The total number of integrated cells and the relative proportion of granule or periglomerular neurons change, according to the donor age, whereas they are weakly influenced by the recipient age. Analysis of the neurochemical phenotypes acquired by transplanted cells in the GL shows that donor cells of different ages also differentiate according to their origin, regardless of the host age. This suggests that progenitor cells at different ontogenetic stages are intrinsically directed toward specific lineages. Neurogenic processes occurring during development and in adult OB are not equivalent and produce different types of periglomerular interneurons as a consequence of intrinsic properties of the SVZ progenitors.

In the corpora allata (CA) of the adult male loreyi leafworm, Mythimna loreyi, juvenile hormone acid (JHA) biosynthesis and release show a dose dependence on extracellular Ca(2+) concentration. Maxima are obtained with Ca(2+) concentrations of 2-10 mM, and synthesis and release are significantly inhibited under a Ca(2+)-free condition. The Ca(2+)-free inhibition of JHA release can be reversed by returning the glands to medium at 5 mM Ca(2+). The cytosolic free Ca(2+) concentration ([Ca(2+)](i)), which was measured with fura-2, in individual CA cells also shows a dose dependence on extracellular Ca(2+) concentration, with significant [Ca(2+)](i) depression being observed in the absence of extracellular Ca(2+). High K(+) significantly increases the JHA release and causes a transient [Ca(2+)](i) increase within seconds in CA cells. High-K(+)-stimulated JHA release is partially inhibited by the benzothiazepine (BTZ)-, dihydropyridine (DHP)- and phenylalkylamine (PAA)-sensitive L-type voltage-dependent calcium channel (VDCC) antagonists diltiazem, nifedipine and verapamil, respectively; by the N- and P/Q-type VDCC antagonist omega-conotoxin (omega-CgTx) MVIIC; and by the T-type VDCC antagonist amiloride. The N-type antagonist omega-CgTx GVIA is the most potent in inhibiting the high-K(+)-stimulated JHA release. No inhibitory effect is shown by the P-type antagonist omega-agatoxin TK (omega-Aga TK). The high-K(+)-induced transient [Ca(2+)](i) increase is largely inhibited by the L-type antagonists (diltiazem, nifedipine, verapamil), by the N- and P/Q-type antagonist omega-CgTx MVIIC and by the T-type antagonist amiloride, and is totally inhibited by the N-type antagonist omega-CgTx GVIA. No inhibitory effect is shown by the P-type antagonist omega-Aga TK. We hypothesize that L-type, N-type and T-type VDCCs may be involved to different degrees in the high-K(+)-stimulated JHA release and transient [Ca(2+)](i) increase in the individual CA cells of the adult male M. loreyi, and that the N-type VDCCs may play important roles in these cellular events.

For firefighters and rescuers, the disaster relief works are difficulty performed in the tunnels because of their constricted space. To reduce the losses of accident, the safety of tunnels and factories should be ordinarily kept under surveillance. Hence, a multisensor based smart tracked vehicle is designed for the application of autonomous detection and surveillance in this paper. Besides, multisensors, communication modules, wireless cameras, an electronic compass, and a GPS module are installed in the vehicle. The key feature is the integration of disaster detection and warning systems so that the vehicle can move autonomously. Furthermore, a LabVIEW graphical programming software is applied to design a human machine interface (HMI) and integrate all systems such that the vehicle can be guided by High Speed Downlink Packet Access (HSHPA) based remote control. Moreover, basic stamp microcontrollers are utilized as its control kernel such that the remote monitoring and control system (RMCS) can be constructed successfully.

A low driving voltage and fast response blue phase III (BPIII) liquid-crystal device with very low dielectric anisotropy is demonstrated. To stabilize BPIII in a wide temperature range (> 15°C), a chiral molecule with good solubility was chosen. By studying field-dependent polarization state of the transmitting light, it was found that the field-induced birefringence becomes saturated in the high field. However, the transmitting intensity exhibits a tendency to increase as the electric field increases. This indicates that the electro-optical behavior in BPIII device may be from the flexoelectric effect, which induces tilted optical axis and then induces birefringence. Because the phase transition from BPIII to chiral nematic phase does not happen, the device shows no hysteresis effect and no residual birefringence, exhibits fast response, and can be a candidate for fast photonic application.

As one of the major steps toward fully intelligent autonomous robotic weapon, this paper works have accomplished in three major areas: (1) design of the surveillance system by 89C51 microcomputers, (2) implementation of the obstacle avoidance system, and (3) performance of the human machine interface surveillance system via LabVIEW graphical programming environment and wireless network surveillance equipment, such that the supervisor can control the vehicle by keyboard or genius mouse. In order to accomplish all these three achievements, there have been major additions and overhaul in both system software code and system circuit board developments. All these development including the developed algorithm, and hardware implementation are covered in this paper. The experimental results have shown the practicality of the 89C51 microcomputer, obstacle avoidance systems, LabVIEW graphical programming environment, wireless network surveillance equipment, and the ZigBee wireless technology applied to weapon robots.

In ultrasonic harmonic imaging, the contrast-to-tissue ratio (CTR) is generally limited by tissue background signal comprising both the leakage harmonic signal and the tissue harmonic signal. In this paper, suppression of tissue background signal in harmonic imaging is studied by selecting an optimal phase of the transmit signal to achieve destructive cancellation between the tissue harmonic signal and the leakage harmonic signal. With the optimal suppression phase, our results indicate that the tissue signal can be significantly reduced at second harmonic band while the harmonic amplitude from contrast agents shows negligible change. Consequently, CTR improvement can be achieved using optimal transmit phase tuning.

Tissue harmonic imaging suffers from low signal-to-noise ratio (SNR) under typical imaging conditions. On the contrary, presence of strong tissue harmonics also degrades microbubble detection in contrast harmonic imaging. Therefore, a novel approach for both enhancement and suppression of tissue harmonic signal is developed by phasing transmit signal at 3f 0 frequency. Results indicate that the relative phasing between the frequency-sum component and the frequency-difference component markedly changes the amplitude of the second harmonic signal over a wide range of axial depths. For harmonic enhancement, approximate 6 dB increase of second harmonic amplitude can be achieved with improved lateral harmonic beam pattern. For harmonic suppression, the second harmonic signal can be significantly reduced by about 11 dB. Hence, the method of 3f 0 transmit phasing has potentials both for improving SNR in tissue harmonic imaging and for enhancing image contrast in contrast agent imaging by suppression of tissue harmonic background.

This paper presents a quick monitor method to measure micro height variations directly. Here we apply optical moiré technology with a program designed by ourselves to Traditional Chinese Medical Pulse diagnosis. We analyze the moiré pattern which records the information of pulse, and then examine the conditions of pulse, the conditions of pulse including the location of pulse (by image processing the moiré pattern), the rhythm of pulse (via the frequency), the shape of pulse (via moiré pattern) and the strength of pulse (via amplitude intensity). Therefore, we can quantify the conditions of pulse by the system.

In allergic patients sensitive to house dust mite allergens, the inhaled allergenic proteins are dissolved in mucosal fluid, cross mucosal epithelia of the airway, and induce crosslinking of FcεRI-bound allergen-specific IgE on mast cells and basophils, leading to the degranulation of those inflammatory cells. Our group has proposed that allergen-specific IgG, delivered to the airway mucosa, can bind to the incoming allergens and preclude their entry into the mucosal layer. In this work, we prepared human monoclonal antibodies by isolating dust mite allergen-specific single B cells from patients with atopic dermatitis and performing PCR on the VH and VL cDNA of the B cells. One mAb, 1D11, an IgG1 (γ1, λ), bound strongly to both Der p 2 and Der f 2 and recognized a linear epitope in the peptide segment, a.a. residues #41-70, of the two proteins. We proceeded evaluating the ability of 1D11 to trap Der p 2 and Der f 2 in a culture of rat basophilic leukemic (RBL) SX-38 cells, which were charged with allergen-specific IgE contained in patient sera. In the culture, 1D11 was capable of inhibiting the degranulation of RBL SX-38 cells triggered by Der p 2 and Der f 2. Furthermore, the activation was reduced to the background level when protein A-conjugated Sepharose was employed to remove the 1D11-allergen complexes. These results indicate that mAb 1D11 is effective in trapping Der p 2 and Der f 2 allergens and prevent their activation of allergen-specific IgE-sensitized basophils.

The effects of voltage-dependent calcium channel (VDCC) antagonists and the non-specific calcium channel antagonists on both juvenile hormone acids (JHA) release and cytosolic free calcium concentration ([Ca2+]i) are investigated in the corpora allata (CA) of the adult males loreyi leafworm Mythimna loreyi. The VDCC antagonists used in this study are: the L-type antagonists diltiazem, nifedipine, and verapamil, the N-type antagonist ω-Conotoxin (CgTx) GVIA, the N- and P/Q-type antagonist ω-CgTx MVIIC, and the T-type antagonist amiloride. The non-specific calcium channel antagonists used in this study were cadmium (Cd2+), cobalt (Co2+), nickle (Ni2+), and lanthanum (La3+). The results show that both the DHPs-sensitive L-type antagonist nifedipine and the N-type antagonist ω-CgTx GVIA were able to inhibit JHA release, but only ω-CgTx GVIA was able to reduce the [Ca2+]i. Among the non-specific calcium channel antagonists, Cd2+ is the most potent in reducing JHA release but without obvious effect on the [Ca2+]i, La3+ significantly increases the [Ca2+]i but without effect on JHA release. Arch. Insect Biochem. Physiol. 48:89–99, 2001. © 2001 Wiley-Liss, Inc.